Tetrandrine may protect against lung fibrosis by inducing autophagy, according to a new study published in the journal Frontiers in Pharmacology. This finding by Chinese researchers suggests it could potentially be used as a novel therapeutic against idiopathic pulmonary fibrosis (IPF).

IPF is characterized by interstitial remodeling leading to the formation of scar tissue in the lungs. There is currently no cure for IPF and the only 2 drugs approved to treat the disease, pirfenidone and nintedanib, cannot stop its progression. So there is a high unmet clinical need for IPF.

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Here, a team of researchers from the Department of Respiratory and Critical Care Medicine, Chronic Airways Diseases Laboratory, Nanfang Hospital, Southern Medical University, in Guangzhou China evaluated the potential therapeutic effects of tetrandrine against pulmonary fibrosis. Tetrandrine is a low-toxicity drug extracted from the plant Stephania tetrandra S. Moore and a monomeric component of traditional Chinese medicine. Previous research has shown it has antifibrotic effects and induces autophagy.

The team used a mouse model of IPF as well as lung fibroblasts grown in culture to evaluate the antifibrotic effects of tetrandrine. The results showed it decreased the expression of α-smooth muscle actin, fibronectin, vimentin, and type 1 collagen and, therefore, proliferation in fibroblasts. 

Tetrandrine also induced autophagy and suppressed the expression of fibrotic markers and improved lung function in the mice.

“Our data suggest that protective effect of tetrandrine against lung fibrosis might be through promoting . . . autophagy,” the researchers wrote. “Tetrandrine may thus be potentially employed as a novel therapeutic medicine against IPF.”

More research is needed to confirm the antifibrotic effects of tetrandrine before it can be considered as a therapeutic agent in humans.

Reference

Liu Y, Zhong W, Zhang J, et al. Tetrandrine modulates Rheb-mTOR signaling-mediated selective autophagy and protects pulmonary fibrosis. Front Pharmacol. 2021;22;12:739220. doi:10.3389/fphar.2021.739220